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Key Documents

SAB4300213

Sigma-Aldrich

Anti-phospho-H2AFX (pSer139) antibody produced in rabbit

affinity isolated antibody

Synonyme(s) :

Anti-H2A histone family, member X antibody produced in rabbit, Anti-H2A.X antibody produced in rabbit, Anti-H2A/X antibody produced in rabbit, Anti-H2AX antibody produced in rabbit

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About This Item

Numéro MDL:
MFCD07370338
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

~15 kDa

Espèces réactives

human

Concentration

1 mg/mL

Technique(s)

indirect immunofluorescence: 1:100-1:200
western blot: 1:500-1:1000

Isotype

IgG

Séquence immunogène

(Q-A-SP-Q-E)

Numéro d'accès NCBI

NP_002096.1

Numéro d'accès UniProt

P16104

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

phosphorylation (pSer139)

Informations sur le gène

human ... H2AFX(3014)

Immunogène

Peptide sequence around phosphorylation site of serine 139 (Q-A-S(p)-Q-E), according to the protein H2AFX.

Caractéristiques et avantages

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Description de la cible

Variant histone H2A which replaces conventional H2A in a subset of nucleosomes. Nucleosomes wrap and compact DNA into chromatin, limiting DNA accessibility to the cellular machineries which require DNA as a template. Histones thereby play a central role in transcription regulation, DNA repair, DNA replication and chromosomal stability. DNA accessibility is regulated via a complex set of post-translational modifications of histones, also called histone code, and nucleosome remodeling. Required for checkpoint-mediated arrest of cell cycle progression in response to low doses of ionizing radiation and for efficient repair of DNA double strand breaks (DSBs) specifically when modified by C-terminal phosphorylation.

Forme physique

Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

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Anticorps anti-phospho-histone H2A.X (Ser139), clone JBW301 clone JBW301, Upstate®, from mouse

Sigma-Aldrich

05-636

Anticorps anti-phospho-histone H2A.X (Ser139), clone JBW301

Thomas Mathivet et al.
EMBO molecular medicine, 9(12), 1629-1645 (2017-10-19)
Glioma growth and progression are characterized by abundant development of blood vessels that are highly aberrant and poorly functional, with detrimental consequences for drug delivery efficacy. The mechanisms driving this vessel dysmorphia during tumor progression are poorly understood. Using longitudinal
Yixuan Zhang et al.
Gene, 711, 143949-143949 (2019-07-01)
As a transcriptional repressor, Chromobox 8 (CBX8) overexpression is found to be associated with tumorigenesis in several cancers. However, its role in radiotherapy resistance remains poorly characterized. Our study is the first to explore the correlation between CBX8 and radioresistance.
Chen Qu et al.
Journal of cellular and molecular medicine, 21(11), 2872-2883 (2017-05-31)
Radioresistance-induced residual and recurrent tumours are the main cause of treatment failure in nasopharyngeal carcinoma (NPC). Thus, the mechanisms of NPC radioresistance and predictive markers of NPC prognosis and radioresistance need to be investigated and identified. In this study, we
Hui Xiao Chao et al.
Cell systems, 5(5), 445-459 (2017-11-06)
Although molecular mechanisms that prompt cell-cycle arrest in response to DNA damage have been elucidated, the systems-level properties of DNA damage checkpoints are not understood. Here, using time-lapse microscopy and simulations that model the cell cycle as a series of
Fabiana M Meliso et al.
Oncotarget, 8(70), 114540-114553 (2018-02-01)
In a murine melanoma model, malignant transformation promoted by a sustained stress condition was causally related to increased levels of reactive oxygen species resulting in DNA damage and massive epigenetic alterations. Since the chromatin modifier Sirtuin-1 (SIRT1) is a protein
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